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Acute respiratory distress syndrome: A rare presentation of amantadine toxicity

Patient: Male, 64 Final Diagnosis: Acute Respiratory Distress Syndrome (ARDS) Symptoms: Generalized myoclonic jerks • impaired concentration • memory decline • visual hallucinations Medication: Amantadine HCl Clinical Procedure: — Specialty: Toxicology OBJECTIVE: Adverse events of drug therapy BACKG...

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Autores principales: Cattoni, Juan, Parekh, Ravish
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890401/
https://www.ncbi.nlm.nih.gov/pubmed/24427376
http://dx.doi.org/10.12659/AJCR.889931
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author Cattoni, Juan
Parekh, Ravish
author_facet Cattoni, Juan
Parekh, Ravish
author_sort Cattoni, Juan
collection PubMed
description Patient: Male, 64 Final Diagnosis: Acute Respiratory Distress Syndrome (ARDS) Symptoms: Generalized myoclonic jerks • impaired concentration • memory decline • visual hallucinations Medication: Amantadine HCl Clinical Procedure: — Specialty: Toxicology OBJECTIVE: Adverse events of drug therapy BACKGROUND: Amantadine is indicated for treatment of influenza A infection, Parkinson disease and extrapyramidal reactions. Amantadine overdose affects mainly cardiovascular and central nervous systems. Amantadine-induced respiratory failure has not been described in previous case reports but it is a potential known side effect. CASE REPORT: We describe the case of a 64-year-old African American male with end stage renal disease who was prescribed amantadine at a dose for normal kidney function (300 milligrams per day) for no clear reasons. Patient’s serum level of amantadine drawn on admission was found to be 6200 nanogram per deciliter (ng/dl) with normal range being 700–1000 ng/dl. Amantadine hydrochloride is not actively metabolized in humans; is mainly excreted unchanged in urine by glomerular filtration and tubular secretion (90% of the ingested dose). It tends to accumulate in patients with impaired renal function; poorly excreted in patients on hemodialysis and has a large volume of distribution. CONCLUSIONS: Our patient with impaired renal function was prescribed a much higher dose and eventually presented with high serum concentration of amantadine and neurological manifestations suggestive of amantadine toxicity. He developed sudden onset respiratory failure and pulmonary edema which is described as a potential lethal complication of amantadine toxicity. Since there is no specific etiology for his respiratory failure, this could represent the first reported case of Amantadine-induced Adult Respiratory Distress Syndrome (ARDS).
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spelling pubmed-38904012014-01-14 Acute respiratory distress syndrome: A rare presentation of amantadine toxicity Cattoni, Juan Parekh, Ravish Am J Case Rep Articles Patient: Male, 64 Final Diagnosis: Acute Respiratory Distress Syndrome (ARDS) Symptoms: Generalized myoclonic jerks • impaired concentration • memory decline • visual hallucinations Medication: Amantadine HCl Clinical Procedure: — Specialty: Toxicology OBJECTIVE: Adverse events of drug therapy BACKGROUND: Amantadine is indicated for treatment of influenza A infection, Parkinson disease and extrapyramidal reactions. Amantadine overdose affects mainly cardiovascular and central nervous systems. Amantadine-induced respiratory failure has not been described in previous case reports but it is a potential known side effect. CASE REPORT: We describe the case of a 64-year-old African American male with end stage renal disease who was prescribed amantadine at a dose for normal kidney function (300 milligrams per day) for no clear reasons. Patient’s serum level of amantadine drawn on admission was found to be 6200 nanogram per deciliter (ng/dl) with normal range being 700–1000 ng/dl. Amantadine hydrochloride is not actively metabolized in humans; is mainly excreted unchanged in urine by glomerular filtration and tubular secretion (90% of the ingested dose). It tends to accumulate in patients with impaired renal function; poorly excreted in patients on hemodialysis and has a large volume of distribution. CONCLUSIONS: Our patient with impaired renal function was prescribed a much higher dose and eventually presented with high serum concentration of amantadine and neurological manifestations suggestive of amantadine toxicity. He developed sudden onset respiratory failure and pulmonary edema which is described as a potential lethal complication of amantadine toxicity. Since there is no specific etiology for his respiratory failure, this could represent the first reported case of Amantadine-induced Adult Respiratory Distress Syndrome (ARDS). International Scientific Literature, Inc. 2014-01-02 /pmc/articles/PMC3890401/ /pubmed/24427376 http://dx.doi.org/10.12659/AJCR.889931 Text en © Am J Case Rep, 2014 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License
spellingShingle Articles
Cattoni, Juan
Parekh, Ravish
Acute respiratory distress syndrome: A rare presentation of amantadine toxicity
title Acute respiratory distress syndrome: A rare presentation of amantadine toxicity
title_full Acute respiratory distress syndrome: A rare presentation of amantadine toxicity
title_fullStr Acute respiratory distress syndrome: A rare presentation of amantadine toxicity
title_full_unstemmed Acute respiratory distress syndrome: A rare presentation of amantadine toxicity
title_short Acute respiratory distress syndrome: A rare presentation of amantadine toxicity
title_sort acute respiratory distress syndrome: a rare presentation of amantadine toxicity
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890401/
https://www.ncbi.nlm.nih.gov/pubmed/24427376
http://dx.doi.org/10.12659/AJCR.889931
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